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prostaglandin/seizures

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Leht 1 alates 270 tulemused

Galangin Prevents Increased Susceptibility to Pentylenetetrazol-Stimulated Seizures by Prostaglandin E2.

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Epilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there
Central nervous system (CNS) inflammation in cases such as head trauma, infection and stroke has been associated with the occurrence of epileptic seizures. Microglia, the principal immune cells in the brain, readily become activated in response to injury, infection or inflammation. The bacterial
Accumulating clinical and experimental evidence suggests a role for prostaglandins (PGs) in epilepsy and isolated seizures. Prostaglandin levels are increased in the hippocampus of epileptic patients and in the cerebrospinal fluid of children with febrile seizures. Moreover, increased PGD2, PGE2 and

Prostaglandin-oxytocin induction of mid-trimester abortion complicated by grand mal-like seizures.

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Mid-trimester therapeutic abortion is performed routinely in several clinics by using a combination of intra-amniotic instillation of prostaglandin F2 alpha, followed by intravenous infusion of oxytocin in 5% glucose. In doses as low as 10 mU/min, oxytocin has an antidiuretic action. Two cases of

Modulation of pentylenetetrazol-induced seizures by prostaglandin E2 receptors.

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There is evidence that prostaglandin E2 (PGE2) facilitates the seizures induced by pentylenetetrazol (PTZ), but the role of PGE2 receptors (EPs) in the development of seizures has not been evaluated to date. In the current study we investigated whether selective EP ligands alter PTZ-induced seizures

Prostaglandin E(2) potentiates methylmalonate-induced seizures.

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OBJECTIVE Methylmalonic acidemias are inherited metabolic disorders characterized by methylmalonate (MMA) accumulation and neurologic dysfunction, including seizures. It is known that metabolic crises in affected patients are precipitated by infections. Although growing evidence supports that
The effects of iloprost (ZK 36,374), a new chemically stable analogue of prostacyclin (PGI2), on strychnine-, pentylene-tetrazol-, and maximal electroshock-induced seizures were studied in mice. The time from the beginning of the injection of the convulsant or inducing electroshock to the stage of
COX-2 and prostaglandins (PGs) might play important roles in epilepsy. In kainic acid-induced seizures, the brain largely increases PGD(2), first from COX-1 and later COX-2-induced PGF(2alpha). Pre-treatment with COX-2 inhibitors such as indomethacin, nimesulide, and celecoxib is known to aggravate
Endogenous cerebral prostanoids possess anticonvulsant properties. This study investigates possible age-dependent anomalies of prostanoid synthesis in the brain of seizure-prone DBA/2J (DBA2) mice as compared to sound stimulus-resistant CFLP mice. Irrespective of the age of the animals, a large

Prostaglandin D2 inhibits pentylenetetrazole-induced convulsions in rats by a serotonin-mediated mechanism.

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Prostaglandins (PGs) of the E series are known to exert anticonvulsant action in experimental animals. Earlier studies from this laboratory have indicated that PGE1 inhibits pentylenetetrazole (PTZ)-induced convulsions in rats through a serotonin-mediated mechanism. PGD2, the major PG in the rodent
Cerebrospinal fluid prostaglandin F2 alpha (CSF PGF2 alpha) levels were measured by radioimmunoassay in children as follows: Febrile convulsions (31 cases), epilepsies (32 cases), meningitides (31 cases) and non-neurological diseases (20 cases), totaling 114 cases. A 4.5-fold increase in CSF PGF2
Release of prostaglandins (PGs) from brain tissue increases during experimentally-induced and spontaneous seizures. However, whether PGs or other arachidonic acid metabolites have a role in induction of seizures is still unclear. The effectiveness of pretreatment with PG synthetase inhibitors on

Increased concentration of prostaglandin E-2 in cerebrospinal fluid of children with febrile convulsions.

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Concentrations of prostaglandins (PGs) in the central nervous system are known to increase during and after experimentally induced seizures. In the present study, concentrations of PGE-2 were determined by radioimmunoassay in lumbar cerebrospinal fluid (CSF) of 17 children shortly after a febrile
Excitotoxicity involves over activation of brain excitatory glutamate receptors and has been implicated in neurological, neurodegenerative and neuropsychiatric diseases. Metabolism of arachidonic acid (AA) through the phospholipase A(2) (PLA(2))/prostaglandin-endoperoxide synthase (PTGS) pathway is
Prostaglandin (PG) F(2α) is one of the major prostanoids biosynthesized by cyclooxygenases (COXs) from arachidonic acid. Although it has been reported that there is a selective surge in PGF(2α) production in the hippocampus during kainic acid (KA)-induced seizure activity, the precise
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